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首页> 中文期刊> 《中华医学杂志（英文版）》 >Inhibitory Effects of Sulfur Dioxide on Rat Myocardial Fibroblast Proliferation and Migration

Inhibitory Effects of Sulfur Dioxide on Rat Myocardial Fibroblast Proliferation and Migration

         
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摘要

Background:Myocardial fibrosis is an important pathological change in many heart diseases,but its pathogenesis is very complex and has not yet been fully elucidated.The study was designed to examine whether endogenous sulfur dioxide (SO2) is a novel myocardial fibroblast proliferation and migration inhibitor.Methods:Primary rat myocardial fibroblasts were isolated and transfected with aspartate aminotransferase (AAT1 and AAT2) knockdown lentivirus or empty lentivirus.SO2 content in the supematant was determined with high-performance liquid chromatography,and the expressions ofAAT1,AAT2,proliferating cell nuclear antigen (PCNA),phosphorylated extracellular signal-regulated protein kinase (p-ERK),and total ERK (T-ERK) in the cells were detected.Cell migration was detected by wound healing test.Independent sample t-test (for two groups) and one-way analysis of variance (three or more groups) were used to analyze the results.Results:Both AAT1 and AAT2 knockdown significantly reduced SO2 levels (F =31.46,P ＜ 0.01) and AAT1/2 protein expression (AAT 1,t =12.67,P ＜ 0.01;AAT2,t =9.61,P ＜ 0.01),but increased PCNA expression and Cell Counting Kit-8 (CCK-8) activity as well as the migration in rat primary myocardial fibroblasts (P ＜ 0.01).Supplementation of SO2 rather than pyruvate significantly inhibited the increase in proliferation and migration caused by AAT knockdown (P ＜ 0.01).Mechanistically,the ratio of p-ERK to T-ERK was significantly increased in the AAT1/2 knockdown groups compared with that in the empty lentivirus group (AAT1,t =-7.36,P ＜ 0.01;AAT2,t =-10.97,P ＜ 0.01).Whereas PD98059,an inhibitor of ERK activation,successfully blocked AAT knockdown-induced PCNA upregulation (F =74.01,P ＞ 0.05),CCK-8 activation (F =50.14,P ＞ 0.05),and migration augmentation in myocardial fibroblasts (24 h,F=37.08,P＞ 0.05;48 h,F=58.60,P＞ 0.05).Conclusion:Endogenous SO2 might be a novel myocardial fibroblast proliferation and migration inhibitor via inhibiting the ERK signaling pathway.

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  • 来源
    《中华医学杂志（英文版）》 |2018年第14期|1715-1723|共9页
  • 作者

    Lu-Lu Zhang; Jun-Bao Du; Chao-Shu Tang; Hong-Fang Jin; Ya-Qian Huang;

  • 作者单位

    Department of Pediatrics, Peking University First Hospital, Beijing 100034, China;

    Department of Pediatrics, Peking University First Hospital, Beijing 100034, China;

    Division of Small Molecules and Cardiovascular Disease, Key Laboratory of Molecular Cardiology, Ministry of Education, Beijing 100083, China;

    Department of Physiology and Pathophysiology, Peking University Health Science Centre, Beijing 100091, China;

    Department of Pediatrics, Peking University First Hospital, Beijing 100034, China;

    Department of Pediatrics, Peking University First Hospital, Beijing 100034, China;

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